Fatal pneumonia due to Serratia proteamaculans subsp. quinovora

JOURNAL OF CLINICAL MICROBIOLOGY, Feb. 1993, p. 444 445

Vol. 31, No. 2

0095-1137/93/020444-02$02.00/0 Copyright X 1993, American Society for Microbiology

Fatal Pneumonia Due to Serratia proteamaculans subsp. quinovora CLAUDE BOLLET,1* PATRICK GRIMONT,2 MARC GAINNIER,3 ALAIN GEISSLER,3 JEAN-MARIE SAINTY,3 AND PHILIPPE DE MICCO1 Laboratoire de Microbiologie et d'Hygiene Hospitaliere1 and Service de Reanimation,3 H6pital Salvator, Marseille F13009, and Institut Pasteur, Unite des Enterobacteries,2 Paris F75015, France Received 5 August 1992/Accepted 10 November 1992

Serratia proteamaculans subsp. quinovora was isolated from several samples (blood cultures, tracheal aspirates, pleural effusion) from a patient with pneumonia. This is the first clinical isolate and the first documented human infection caused by this organism.

Serratia liquefaciens has been well known for years in clinical microbiology laboratories, first as Aerobacter liquefaciens, then as Enterobacter liquefaciens, and in the last 15 years as S. liquefaciens (6). Following a DNA hybridization study in 1982, Grimont et al. (7) reported the existence of three groups within the S. liquefaciens group. They proposed two new species, Serratia proteamaculans and Serratia grimesii, the former being divided into two subspecies: Serratia proteamaculans subsp. proteamaculans and Serratia proteamaculans subsp. quinovora (8). S. liquefaciens sensu stricto and S. grimesii have been isolated from clinical samples, most often without clinical significance (4). S. proteamaculans subsp. proteamaculans and S. proteamaculans subsp. quinovora have been isolated from insects, soil, rodents, and plants (4, 5). We report here the first isolation of S. proteamaculans subsp. quinovora from a human clinical specimen. A 43-year-old homeless male alcoholic from the south of France was admitted on 14 June 1990 to an intensive care unit in a Marseille hospital for a large and obstructing abscess of the floor of the mouth following a dental abscess. Treatment with piperacillin (12 g/day) and vancomycin (2 g/day) was started. On 18 June, the patient had a tracheotomy because of his suffocating abscess. The abscess site was then incised (no samples for culture were taken). In the immediate postoperative period, the patient showed signs of respiratory distress which was perhaps due to the inhalation of pus. On 24 June, he presented with a purulent left pleural effusion that required the insertion of a drain. He also had digestive hemorrhaging because of a peptic ulcer esophagitis. On 28 June, a computed tomography scan revealed a pneumonia in the right lung with a septated right pleural effusion and extension to the right superior mediastinum. On the same day, a gram-negative bacterium was isolated in pure culture and in great quantity from a bronchial aspirate and a pleural effusion sample. This bacterium was identified in our laboratory as S. proteamaculans. On 2 July, the same bacterium was isolated from two drains (left and right sides) and from two sets of blood cultures. Approximately 1 liter of pus was drained. The numerous false membranes required the positioning of four thoracic and two mediastinal Delbey drains. S. proteamaculans was again isolated from bronchial aspirates on 9 and 12 July. On 13 July, the patient presented *

with a cholecystitis requiring exploratory laparotomy. At that time, a chronic calcifying pancreatitis was observed. A cholecystectomy was performed. A hepatic biopsy revealed a cirrhosis with steatosis. On the next day, the hemodynamic and respiratory conditions of the patient worsened. On 16 July, Kiebsiella pneumoniae and Pseudomonas aeruginosa were isolated from bronchial aspirates. On the same day, S. proteamaculans was again isolated from a central veinous catheter (106 CFU/cm of catheter). On July 17, a cervicothoracic computed tomography scan revealed a bilateral pneumonia without mediastinal gathering. On the same day, acute renal failure was observed. Despite renal dialysis, the patient died on 18 July of multiple-organ failure. After 24 h, a culture of the isolated organism showed smooth colonies on Mueller-Hinton agar (bioMerieux, Marcy-l'Etoile, France). The strain had a biochemical profile number of 5 307 563 when tested by the API 20E system (bioMerieux). The 1992 edition of the API Index gives for this profile "excellent identification to the genus Serratia," but the data matrix of the API 20E identification system did not contain the species of the S. liquefaciens group. The organism was identified as S. proteamaculans subsp. quinovora by the TAXIDEN numerical identification program (Intelligence Artificielle Applications, Clapiers, France), which computes the probability products and standardized Lapage identification score (1). Multiple biochemical tests were subsequently performed, as described earlier (2), to confirm the identification of the organism. Identification was confirmed by using carbon source utilization tests as described earlier (3). All biochemical test cultures were incubated for 72 h at 30°C. The organism was positive for catalase, lysine decarboxylase (Moeller), ornithine decarboxylase (Moeller), Voges-Proskauer reaction, DNase, gelatin liquefaction, and Tween 80 esterase but was negative for oxidase, indole, urease, and arginine hydrolysis. The organism utilized the following compounds as sole sources of carbon and energy: N-acetyl-D-glucosamine, L-arabinose, cellobiose, D-lyxose, raffinose, D-sorbitol, sucrose, D-turanose, L-tyranosine, and D-xylose. The organism did not utilize adonitol, i-erythritol, D-glucosamine, D-quinate, Lrhamnose, trigonelline, or xylitol. The MICs of 17 antibiotics for the organism were determined by the agar dilution method, as described by the National Committee for Clinical Laboratory Standards, by using cation-supplemented Mueller-Hinton medium (bioMerieux). The isolate was found to be susceptible to cefotaxime (MIC, 0.025 p,g/ml), cefotiam (MIC, 2 ,ug/ml), ceftri-

Corresponding author. 444

VOL. 31, 1993 axone (MIC, 0.12 ,ug/ml), piperacillin (MIC, 0.12 ,ug/ml), imipenem (MIC, 0.12 ,ug/ml), tobramycin (MIC, 0.25 jig/ml), amikacin (MIC, 0.5 ,ug/ml), netilmicin (MIC, 0.12 ,ug/ml), ofloxacin (MIC, 0.12 ,ig/ml), pefloxacin (MIC, 0.25 jig/ml), and ciprofloxacin (MIC, 0.012 ,ug/ml). The isolate was resistant to ampicillin (MIC, 64 jig/ml), ampicillin-clavulanic acid (MIC, 32 ,ug/ml), cefoxitin (MIC, 256 jig/ml), erythromycin (MIC, 64 jig/ml), doxycycline (MIC, 256 jig/ml), and fosfomycin (MIC, 32 jig/ml). Because no other causative agent was found, the pneumonia described here seems to have been caused by the isolated S. proteamaculans strain. No other S. liquefaciens group infection was noted in the same ward or the entire hospital during this period. Given the patient's life-style, this Serratia strain may well have been acquired while he slept on the ground outside. To our knowledge, this is the first documented human infection caused by S. proteamaculans subsp. quinovora.

NOTES

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We thank N. Cassar and M. Moya for technical assistance.

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